Experimental allergic encephalomyelitis (EAE), a model autoimmune disease is being used to study immune reactivity and inflammation in the central nervous system (CNS). Current research is focused on a chronic-relapsing experimental disease produced in syngeneic animals by the transfer of lymphocytes sensitized against myelin basic protein. The neurological dysfunction is characterized pathologically by inflammation and primary demyelination. The immunological mechanisms responsible for the initial episode and the chronic disease are being investigated. An early event is the migration of immune cells across the blood-brain barrier into the CNS. The effect of various cytokines is being studied in order to gain insight to the pathogenic mechanisms involved and to provide rationale for experimental treatments. The administration of transforming growth factor-beta (TGF-beta) prior to the onset of disease reduces the intensity of the initial episode. When given after the first episode, the subsequent course is significantly less severe. The administration of another cytokine, interferon-gamma (IFN-gamma), also inhibits the initial episode, and it is possible that IFN-gamma increases the endogenous expression of TGF-beta. After the transfer of disease-inducing T cells, there is interaction with the capillary endothelial cells, but astrocytes and microglia are in close proximity. Antigen presentation by microglia, brain capillary endothelial, and astrocytes are being compared. The expression of MHC molecules in these cells and the influence of TGF-beta and IFN-gamma on these molecules is being evaluated using cultures of murine fetal CNS cells, adult human glia cells, and murine brain capillary endothelial cells. Expression and regulation of MHC molecules by neurons is also being examined.